Substance Abuse
Objectives
When you reach the end of this chapter, you will be able to do the following:
1 Discuss substance abuse and the significance of the problem in the United States.
2 Identify the drugs or chemicals that are most frequently abused.
3 Contrast the signs and symptoms of the most commonly abused drugs/chemicals.
7 Identify various assessment tools used in the nursing assessment of substance abuse.
Key Terms
Addiction Strong psychological or physical dependence on a drug or other psychoactive substance. (p. 282)
Amphetamine A drug that stimulates the central nervous system. (p. 284)
Detoxification A process of eliminating a toxic substance from the body; a medically supervised program for alcohol or opioid addiction (p. 284)
Enuresis Urinary incontinence. (p. 285)
Habituation Development of tolerance to a substance following prolonged medical use but without psychological or physical dependence (addiction). (p. 282)
Illicit drug use The use of a drug or substance in a way that it is not intended to be used or the use of a drug that is not legally approved for human administration. (p. 284)
Intoxication Stimulation, excitement, or stupefaction produced by a chemical substance. (p. 282)
Korsakoff’s psychosis A syndrome of amnesia with confabulation (making up of stories) associated with chronic alcohol abuse; it often occurs together with Wernicke’s encephalopathy. (p. 287)
Micturition Urination, the desire to urinate, or the frequency of urination. (p. 285)
Narcolepsy A sleep disorder characterized by sleeping during the day, disrupted nighttime sleep, cataplexy, sleep paralysis, and hallucinations. (p. 285)
Opioid analgesics Synthetic pain-relieving substances that were originally derived from the opium poppy. Naturally occurring opium derivatives are called opiates. (p. 283)
Physical dependence A condition characterized by physiologic reliance on a substance, usually indicated by tolerance to the effects of the substance and development of withdrawal symptoms when use of the substance is terminated. (p. 282)
Psychoactive properties Drug properties that affect mood, behavior, cognitive processes, and mental status. (p. 284)
Psychological dependence A condition characterized by strong desires to obtain and use a substance. (p. 282)
Raves Increasingly popular all-night parties that typically involve dancing, drinking, and the use of various illicit drugs. (p. 285)
Roofies Pills that are classified as benzodiazepines. They have recently gained popularity as a recreational drug; chemically known as flunitrazepam. (p. 286)
Substance abuse The use of a mood- or behavior-altering substance in a maladaptive manner that often compromises health, safety, and social and occupational functioning, and causes legal problems. (p. 282)
Wernicke’s encephalopathy A neurologic disorder characterized by apathy, drowsiness, ataxia, nystagmus, and ophthalmoplegia; it is caused by thiamine (vitamin B1) deficiency secondary to chronic alcohol abuse. (p. 287)
Withdrawal A substance-specific mental disorder that follows the cessation or reduction in use of a psychoactive substance that has been taken regularly to induce a state of intoxication. (p. 282)
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Anatomy, Physiology, and Pathophysiology Overview
Substance abuse affects people of all ages, sexes, and ethnic and socioeconomic groups. Physical dependence and psychological dependence on a substance are chronic disorders with remissions and relapses, such as occur with any other chronic illness. Relapses are not to be seen as failures but as indications to intensify treatment. Recognizing physical or psychological dependence and understanding the various treatment guidelines are important skills for those caring for these patients. Habituation refers to situations in which a patient becomes accustomed to a certain drug (develops tolerance) and may have mild psychological dependence on it but does not show compulsive dose escalation, drug-seeking behavior, or major withdrawal symptoms on drug discontinuation. This might occur, for example, in a postsurgical patient who receives opioid pain therapy regularly for only a few weeks.
In 2010, the Office of Applied Studies of the U.S. Substance Abuse and Mental Health Services Administration conducted a survey indicating that some 22.6 million Americans 12 years of age or older were current illicit drug users; that is, they reported using an illicit drug during the month prior to the survey interview. This number represents 8.9% of the population 12 years of age and older. Marijuana was identified as the most commonly used illicit drug, followed by psychotherapeutic drugs, pain relievers, tranquilizers, stimulants, and sedatives used for nonmedical purposes.
Nearly 50% of the adult patients seen in many family practice clinics have an alcohol or drug disorder. Some 25% to 40% of hospital admissions are related to substance abuse and its sequelae. Of patients seen in a general medicine practice, 10% to 16% are seeking treatment for problems related to substance abuse. Substance abuse is strongly associated with many types of mental illness. Treatment of both disorders is often very difficult, in part because of the high risk of drug interactions with the abused substances. Assessment, intervention, use of certain medications, specific addiction treatment strategies, and monitoring of recovery are essential to the care of this patient population.
This chapter focuses on three major classes of commonly abused substances and two commonly abused individual drugs. A description of the category or the individual drug, possible effects, signs and symptoms of intoxication and withdrawal, peak period and duration of withdrawal symptoms, and drugs used to treat withdrawal are discussed. The list of substances of abuse in Box 17-1 is not all-inclusive, but it contains some of the substances most commonly abused at this time. Not all of these substances are discussed in this chapter. Refer to The National Institute on Drug Abuse, available at www.nida.nih.gov/nidahome.html for further information.
Specific drugs used to treat withdrawal symptoms are discussed in the sections covering the drug whose withdrawal symptoms they are intended to treat. Pharmacologic therapies are indicated for patients with addictive disorders to prevent life-threatening withdrawal complications, such as seizures and delirium tremens, and to increase compliance with psychosocial forms of addiction treatment.
Pharmacology Overview
Opioids
Opioid analgesics are synthetic versions of pain-relieving substances that were originally derived from the opium poppy plant (see Chapter 10). More than 20 different alkaloids are obtained from the unripe seed of the opium poppy plant, only a few of which are clinically useful, including morphine and codeine. The other opioid analgesics that are currently used in medical practice are synthetic or semisynthetic derivatives of these two drugs.
Diacetylmorphine (better known as heroin) and opium are classified as Schedule I drugs and are not available in the United States for therapeutic use. Heroin was banned in the United States in 1924 because of its high potential for abuse and the increasing number of heroin addicts. In Europe, heroin is available for medical treatment of pain, and governmental programs also exist to provide heroin to addicts with the goal of reducing crime.
Heroin is one of the most commonly abused opioids. Some of the other commonly abused substances in the opioid category are codeine, hydrocodone, hydromorphone, meperidine, morphine, and oxycodone. Currently heroin remains one of the top 10 most abused drugs in the United States and often is used in combination with the stimulant drug cocaine (discussed later in Stimulants). When heroin is injected (called mainlining or skin popping), sniffed (known as snorting), or smoked, it binds with opiate receptors found in many regions of the brain. The result is intense euphoria, often referred to as a rush. This rush lasts only briefly and is followed by a relaxed, contented state that persists for a couple of hours. In large doses, heroin, like other opioids, can reduce or stop respiration.
Mechanism of Action and Drug Effects
Opioids work by blocking receptors in the central nervous system (CNS). When these receptors are blocked, the perception of pain is blocked. There are three main receptor types to which opioids bind. These receptors and their physiologic effects when stimulated are discussed in Chapter 10. One of the reasons that opioids are abused is their ability to produce euphoria.
The drug effects of opioids are primarily centered in the CNS. However, these drugs also act outside the CNS, and many of their unwanted effects stem from these actions. In addition to analgesia, opioids produce drowsiness, euphoria, tranquility, and other alterations of mood. The mechanism by which opioids produce the latter effects is not entirely clear. The effects of opioids can be collectively referred to as narcosis or stupor, which involves reduced sensory response, especially to painful stimuli. For this reason, opioid analgesics are also referred to as narcotics (see Chapter 4), especially by law enforcement authorities.
Indications
The intended drug effects of opioids are to relieve pain, reduce cough, relieve diarrhea, and induce anesthesia. Many have a high potential for abuse and are therefore classified as Schedule II controlled substances. Relaxation and euphoria are the most common drug effects that lead to abuse and psychological dependence. Sustained-release oxycodone (e.g., OxyContin) is an example of an opioid narcotic that is controversial because it is often overprescribed, misused, and grossly abused. Numerous deaths have been reported when sustained-release oxycodone was crushed and the entire 12-hour supply was released at one time.
Certain opioid drugs are themselves used to treat opioid dependence. Historically, methadone has been used most commonly for this purpose. Its long half-life of up to 12 to 24 hours allows patients to be dosed once daily at federally approved methadone maintenance clinics. In theory, the goal of such programs is to reduce the patient’s dosage gradually so that eventually the patient can live permanently drug free. Unfortunately, relapse rates are often high in these programs. However, patients who remain on long-term opioid maintenance therapy still benefit by avoiding the hazards associated with obtaining and using illegal “street” drugs.
Contraindications
Contraindications to the therapeutic use of opioid medications include known drug allergy, pregnancy (high dosage or prolonged use is contraindicated), respiratory depression or severe asthma when resuscitative equipment is not available, and paralytic ileus (bowel paralysis).
Adverse Effects
Adverse effects of opioids can be broken down into two groups: CNS and non-CNS. The primary adverse effects of opioids are related to their actions in the CNS. The major CNS-related adverse effects include diuresis, miosis, convulsions, nausea, vomiting, and respiratory depression. Many of the non-CNS adverse effects are secondary to the release of histamine. Histamine release can cause vasodilation leading to hypotension, spasms of the colon leading to constipation, increased spasms of the ureter resulting in urinary retention, and dilation of cutaneous blood vessels leading to flushing of the skin of the face, neck, and upper thorax. The release of histamine is also thought to cause sweating, urticaria, and pruritus.
Management of Withdrawal, Toxicity, and Overdose
Box 17-2 lists the signs and symptoms of opioid withdrawal. The box also indicates the time when these symptoms are most likely to occur and their duration. Many patients require a formal detoxification program while withdrawal symptoms are occurring. See Chapter 10 for a detailed discussion of physical dependence and the management of acute intoxication, toxicity, and overdose. Withdrawal symptoms include nausea, dysphoria, muscle aches, lacrimation, rhinorrhea, pupillary dilation, piloerection (hair standing on end) or sweating, diarrhea, yawning, fever, and insomnia. Medications listed in Box 17-3 are intended to help decrease the desire for the abused opioid and reduce the severity of these withdrawal symptoms. The most serious adverse effect and the most common cause of death with opioids is respiratory depression.
Certain medications are used to prevent relapse use once an initial remission is achieved. They are useful only when concurrent counseling is provided and offer additional insurance against return to illicit drug use. For opioid abuse or dependence, naltrexone, an opioid antagonist, is administered. Naltrexone, which is also available as an injection called Vivitrol, works by blocking the opioid receptors so that use of opioid drugs does not produce euphoria. When euphoria is eliminated, the reinforcing effect of the drug is lost. The patient needs to be free from opioids for at least 1 week before beginning this medication, because naltrexone can produce withdrawal symptoms if given too soon. Naltrexone is also approved for use by alcohol-dependent patients to reduce cravings for alcohol and the likelihood of a full relapse if a slip occurs. Another opioid antagonist, naloxone, is used for opioid dependence. It is combined with buprenorphine (Subutrex) or used alone (Suboxone) (see Chapter 10).
Stimulants
The abuse of stimulants is related to their ability to cause elevation of mood, reduction of fatigue, a sense of increased alertness, and invigorating aggressiveness. Amphetamine is a stimulant drug that is commonly abused. Chemically, three classes of amphetamine exist: salts of racemic amphetamine, dextroamphetamine, and methamphetamine. These classes vary with respect to their potency and peripheral effects. Another stimulant drug of abuse is cocaine, which also produces strong CNS stimulation. Cocaine was originally classified as a narcotic. It is considered a narcotic by the penal system and has been treated as a narcotic in terms of secured storage in health care facilities. However, unlike the opioid analgesics, cocaine does not normally induce a state of narcosis or stupor and is therefore more correctly categorized as a stimulant drug. Other commonly abused substances in this category include methylphenidate, dextroamphetamine, phenmetrazine, and methamphetamine. Multiple slight chemical variants of amphetamine exist. They are commonly referred to as “designer drugs,” which have psychoactive properties along with their stimulant properties, which further enhances their abuse potential. Table 17-1 lists commonly abused forms of amphetamine and cocaine with their street names.
TABLE 17-1
VARIOUS FORMS OF AMPHETAMINE AND COCAINE WITH STREET NAMES
| CHEMICAL NAME | STREET NAMES |
| dimethoxymethylamphetamine | DOM, STP |
| methamphetamine (crystallized form) | Ice, crystal, glass |
| methamphetamine (powdered form) | Speed, meth, crank |
| methylenedioxyamphetamine | MDA, love drug |
| methylenedioxymethamphetamine | MDMA, ecstasy |
| cocaine (powdered form) | Coke, dust, snow, flake, blow, girl |
| cocaine (crystallized form) | Crack, crack cocaine, freebase rocks, rock |
Methamphetamine is a chemical class of amphetamine, but it has a much stronger effect on the CNS than the other two classes of amphetamine. Methamphetamine is generally used in pill form orally or in powder form by snorting or injecting. It has 15 to 20 times the potency of amphetamine sulfate, the original drug in this class. Crystallized methamphetamine, known as ice, crystal, or crystal meth, is a smokable and more powerful form of the drug. Methamphetamine users who inject the drug and share needles are at risk for acquiring human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS), as well as hepatitis B and C. Marijuana and alcohol are commonly listed as additional drugs of abuse in those admitted for treatment of methamphetamine abuse. Most of the recorded methamphetamine-related deaths involved the use of methamphetamine in combination with at least one other drug, such as alcohol, heroin, or cocaine. The over-the-counter (OTC) decongestant pseudoephedrine is commonly used to synthesize methamphetamine in secret drug laboratories, often in private homes. This practice has lead to dramatic increases in the abuse of this drug. In 2005, the Combat Methamphetamine Epidemic Act required restricted retail sales of all nonprescription drug products containing pseudoephedrine. Specific restrictions include allowing sales only from behind the pharmacy counter, requiring photo identification and electronic or paper record keeping of purchasers (which must remain on file for 2 years), and setting maximum allowable amount (in grams) of pseudoephedrine that can be sold per consumer per month.
Another synthetic amphetamine derivative is methylenedioxymethamphetamine (MDMA, “ecstasy,” or “E”), which is also usually prepared in secret home laboratories. This drug tends to have more calming effects than other amphetamine drugs. It is usually taken in pill form but can also be snorted or injected. Users often feel a strong sense of social bonding with and acceptance of other people, hence the nickname “love drug.” The drug can also be very energizing, which makes it popular at raves (all-night dance parties). Originally synthesized by Merck Pharmaceuticals in 1914, it was studied by the U.S. Army as a “brainwashing” drug in the 1950s. Its popularity has grown widely since the Drug Enforcement Administration classified it as a Schedule I controlled substance in 1985.
Another illicit drug use problem is cocaine use. Cocaine is a white powder that is derived from the leaves of the South American coca plant. Cocaine is either snorted or injected intravenously. Cocaine tends to give a temporary illusion of limitless power and energy but afterward leaves the user feeling depressed, edgy, and craving more. Crack is a smokable form of cocaine that has been chemically altered. Cocaine and crack are highly addictive. The psychological and physical dependence can erode physical and mental health and can become so strong that these drugs dominate all aspects of the addict’s life.
Mechanism of Action and Drug Effects
Stimulants work by releasing biogenic amines from their storage sites in the nerve terminals. The primary biogenic amine released is norepinephrine. Its release results in stimulation of the CNS, as well as cardiovascular stimulation, which results in increased blood pressure and heart rate and possibly cardiac dysrhythmias. The effect on smooth muscle is seen primarily in the urinary bladder and results in contraction of the sphincter. This is helpful in treating enuresis (urinary incontinence) but results in painful and difficult micturition (voiding or urination) otherwise.
Stimulants, particularly amphetamines, are very potent CNS stimulants. This CNS stimulation commonly results in wakefulness, alertness, and a decreased sense of fatigue; elevation of mood, with increased initiative, self-confidence, and ability to concentrate; often elation and euphoria; and an increase in motor and speech activity.
Indications
Many therapeutic uses for stimulants exist. Currently their most common use is in the treatment of attention deficit disorder or attention deficit hyperactivity disorder (see Chapter 13). Stimulants may be used to prevent or reverse fatigue and sleep, such as when they are used to treat narcolepsy (episodes of acute sleepiness). Another therapeutic effect of amphetamines is their ability to stimulate the respiratory center. Occasionally they are used after anesthesia to stimulate the respiration. Stimulants are also used to reduce food intake and treat obesity; however, this therapeutic effect is limited because of rapid development of tolerance.
Contraindications
Contraindications to the therapeutic use of stimulant medications include drug allergy, diabetes, cardiovascular disorders, states of agitation, hypertension, known history of drug abuse, and Tourette’s syndrome.
Adverse Effects
Adverse effects of stimulants are commonly an extension of their therapeutic effects. The CNS-related adverse effects are restlessness, syncope (fainting), dizziness, tremor, hyperactive reflexes, talkativeness, tenseness, irritability, weakness, insomnia, fever, and sometimes euphoria. Confusion, aggression, increased libido, anxiety, delirium, paranoid hallucinations, panic states, and suicidal or homicidal tendencies occur, especially in mentally ill patients. Fatigue and depression usually follow the CNS stimulation. Cardiovascular effects are common and include headache, chilliness, pallor or flushing, palpitations, tachycardia, cardiac dysrhythmias, anginal pain, hypertension or hypotension, and circulatory collapse. Excessive sweating can also occur. Gastrointestinal (GI) effects include dry mouth, metallic taste, anorexia, nausea, vomiting, diarrhea, and abdominal cramps. A sometimes fatal hyperthermia can also occur, driven partly by excessive drug-induced muscular contractions.
Management of Withdrawal, Toxicity, and Overdose
Box 17-4 lists the signs and symptoms of withdrawal from stimulants, and also indicates the peak period when these symptoms are most likely to occur and their duration. Death due to poisoning or toxic levels is usually a result of convulsions, coma, or cerebral hemorrhage and may occur during periods of intoxication or withdrawal. Treatment of overdose is supportive and generally requires sedation of the patient.
Depressants
Depressants are drugs that relieve anxiety, irritability, and tension when used as intended. They are also used to treat seizure disorders and induce anesthesia. The two main pharmacologic classes of depressant are benzodiazepines and barbiturates. Both of these drug classes are discussed further in Chapter 12.
Benzodiazepines are relatively safe. They offer many advantages over older drugs used to relieve anxiety and insomnia. However, they are often intentionally and unintentionally misused. Ingestion of benzodiazepines together with alcohol can be lethal. Another depressant that is neither a benzodiazepine nor a barbiturate is marijuana. Derived from the cannabis plant, marijuana (“pot,” “grass,” “weed”) is the most commonly abused drug worldwide. Marijuana is generally smoked as a cigarette (“joint”) or in a pipe (“bong”) but can be mixed in food or tea.
A benzodiazepine that has gained popularity as a recreational drug is flunitrazepam. Flunitrazepam is not legally available for prescription in the United States, but it is legally sold in over 60 countries for treatment of insomnia. The drug, known as roofies among young people, creates a sleepy, relaxed, drunken feeling that lasts 2 to 8 hours. Roofies are commonly used in combination with alcohol and other drugs. They are sometimes taken to enhance a heroin high or to mellow or ease the experience of coming down from a cocaine or crack high. Used with alcohol, roofies produce disinhibition and amnesia.
Roofies have recently gained a reputation as a “date rape” drug. Girls and women around the country have reported being raped after being involuntarily sedated with roofies, which were often slipped into their drinks by their attackers. The drug has no taste or odor, so the victims do not realize what is happening. About 10 minutes after ingesting the drug, the woman may feel dizzy and disoriented, simultaneously too hot and too cold, and nauseous. She may experience difficulty speaking and moving and then pass out. Such a victim will have no memories of what happened while under the influence of the drug. Another popular date rape drug used in similar fashion is gamma-hydroxybutyric acid (GHB). GHB works by mimicking the natural inhibitory brain neurotransmitter gamma-aminobutyric acid (GABA). It is also known as “liquid ecstasy.” These drugs are also used simply for their depressant and hallucinogenic effects.
Mechanism of Action and Drug Effects
Benzodiazepines and barbiturates work by increasing the action of GABA. GABA is an amino acid in the brain that inhibits nerve transmission in the CNS. The alteration of GABA action in the CNS results in relief of anxiety, sedation, and muscle relaxation. The effects of depressants are primarily limited to the CNS. They can also cause amnesia and unconsciousness. They have moderate effects outside the CNS, causing slight blood pressure decreases.
The active ingredients of the marijuana plant are known as cannabinoids, the most active of which is delta-9-trans-tetrahydrocannabinol, abbreviated THC. THC exerts its effects on the body by chemically binding to and stimulating two cannabinoid receptors in the CNS (CB1 and CB2). Smoking the drug leads to acute sensorial changes that start within 3 minutes, peak in 20 to 30 minutes, and last for 2 to 3 hours. Effects are longer when the drug is taken via the oral route. Specific effects include mild euphoria, memory lapses, dry mouth, enhanced appetite, motor awkwardness, and distorted sense of time and space. THC also stimulates sympathetic receptors and inhibits parasympathetic receptors in cardiac tissue, which leads to tachycardia. Other effects include hallucinations, anxiety, paranoia, and unsteady gait.
Indications
Many therapeutic uses of depressants exist. Benzodiazepines are used primarily to relieve anxiety, to induce sleep, to sedate, and to prevent seizures. Barbiturates are used as sedatives and anticonvulsants and to induce anesthesia. Controversial medical uses for marijuana include treatment of chronic pain, reduction of nausea and vomiting associated with cancer treatment, and appetite stimulation in those with wasting syndromes, such as patients with cancer or AIDS. In 1996, California became the first state to legalize the medical use of marijuana. Since that time, 14 other states have legalized the use of marijuana for medical purposes, and others have legislation pending. Dronabinol is a synthetic THC prescription capsule approved by the Food and Drug Administration (FDA) for the previously mentioned indications (see Chapter 52 for further discussion of this drug). However, it is often not popular with those who claim that it is not as effective as inhaled marijuana.
Contraindications
Contraindications to the therapeutic use of depressant medications include known drug allergy, dyspnea or airway obstruction, narrow-angle glaucoma, and porphyria (a metabolic disorder).
Adverse Effects
The most common undesirable effect of benzodiazepines and barbiturates is an overexpression of their therapeutic effects. The CNS is the primary area of the body adversely affected by these drugs. Drowsiness, sedation, loss of coordination, dizziness, blurred vision, headaches, and paradoxical reactions (insomnia, increased excitability, hallucinations) are the primary CNS adverse effects. Occasional GI effects include nausea, vomiting, constipation, dry mouth, and abdominal cramping. Other possible adverse effects are pruritus and skin rash. Long-term use of marijuana may result in chronic respiratory symptoms (similar to those of tobacco abuse) and memory and attention deficit problems. A chronic depressive “amotivational” syndrome has also been observed, especially among younger users.
Management of Withdrawal, Toxicity, and Overdose
Box 17-5 lists the signs, symptoms, and treatment of withdrawal from depressants, and also indicates the peak periods when these symptoms are most likely to occur and their duration. Fatal poisoning is unusual with benzodiazepines when they are taken alone. When benzodiazepines are ingested with alcohol or barbiturates, however, the combination can be lethal. Death is typically due to respiratory arrest. Abrupt withdrawal of benzodiazepines when they have been taken for prolonged periods has resulted in autonomic withdrawal symptoms, seizures, delirium, rebound anxiety, myoclonus (involuntary muscle contractions), myalgia, and sleep disturbances.
Flumazenil is a benzodiazepine reversal agent. Flumazenil antagonizes the action of benzodiazepines on the CNS by directly competing with them for binding at the benzodiazepine receptor in the CNS and thus reversing sedation. The dosage regimen to be followed for the reversal of conscious sedation or general anesthesia induced by a benzodiazepine and the management of suspected benzodiazepine overdoses are summarized in Chapter 12 (Table 12-3).
Barbiturates and benzodiazepines are commonly implicated in suicides, especially in combination with alcohol. Generally speaking, depressants are not regularly prescribed over a long period. Relatively safe hypnotic drugs such as the benzodiazepines are preferred whenever possible, especially in emotionally disturbed patients. Combinations of sedative-hypnotic drugs or in combination with alcohol need to be avoided. Long-term use of hypnotic drugs leads to ineffective control of insomnia, decrease in rapid eye movement sleep, dependence, and drug withdrawal symptoms.
Effects of marijuana use are usually self-limiting and resolve within a few hours.
Alcohol
Alcoholic beverages have been used since the beginning of human civilization. Individuals of Arab descent introduced the technique of distillation to Europe in the Middle Ages. Alcohol has been called the “elixir of life” and has been touted as a remedy for practically all diseases, which led to the use of the term whisky, Gaelic for “water of life.” Over time, it has been determined that the therapeutic value of alcohol is extremely limited, and long-term ingestion of excessive amounts is a major social and medical problem.
Mechanism of Action and Drug Effects
Alcohol, which is more accurately known as ethanol and abbreviated as ETOH, is a CNS depressant. It results in CNS depression by dissolving in the lipid membranes within the CNS. The latest hypothesis is that ethanol causes a local disordering in the lipid matrix of the brain. This has been termed membrane fluidization. Some also believe that ethanol may augment GABA-mediated synaptic inhibition and fluxes of chloride. This enhancement of the action of GABA, an inhibitory neurotransmitter in the brain, causes CNS depression. The CNS is continuously depressed in the presence of ethanol. Moderate amounts of ethanol may stimulate or depress respirations. Effects of ethanol on the circulation are relatively minor. In moderate doses, ethanol causes vasodilation, especially of the cutaneous vessels, and produces warm, flushed skin. Ingestion of ethanol causes a feeling of warmth because it enhances cutaneous and gastric blood flow. Increased sweating may also occur. Heat is therefore lost more rapidly, and the internal body temperature consequently falls. The short-term (versus long-term) ingestion of ethanol, even in intoxicating doses, produces little lasting change in hepatic function. Long-term ingestion of ethanol is one of the primary causes of liver failure. Ethanol exerts a diuretic effect by virtue of its inhibition of antidiuretic hormone secretion and the resultant decrease in renal tubular reabsorption of water.
Indications
Few legitimate uses of ethanol and alcoholic beverages exist. Ethanol is an excellent solvent for many drugs and is commonly employed as a vehicle for medicinal mixtures. When applied topically to the skin, ethanol acts as a coolant. Ethanol sponges are therefore used to treat fever. Ethanol may also be used in liniments (oily medications used on the skin). Applied topically, ethanol is the most popular skin disinfectant. More commonly, however, the type of alcohol used on the skin is isopropyl alcohol, which is similar in structure to ethanol but is more toxic and is not drinkable.
Systemic uses of ethanol are limited to the treatment of methyl alcohol and ethylene glycol intoxication (e.g., from drinking automotive antifreeze solution). However, small amounts of ethanol preparations (such as red wine) have been shown to have cardiovascular benefits.
Adverse Effects
Long-term excessive ingestion of ethanol is directly associated with serious neurologic and mental disorders. These neurologic disorders can result in seizures. Nutritional and vitamin deficiencies, especially of the B vitamins, can occur and can lead to Wernicke’s encephalopathy, Korsakoff’s psychosis, polyneuritis, and nicotinic acid deficiency encephalopathy.
Moderate amounts of ethanol may stimulate or depress respirations. Large amounts produce dangerous or lethal depression of respiration. Although circulatory effects of ethanol are relatively minor, acute severe alcoholic intoxication may cause cardiovascular depression. Long-term excessive use of ethanol has largely irreversible effects on the heart, such as cardiomyopathy.
When consumed on a regular basis in large quantities, ethanol produces a constellation of dose-related negative effects such as alcoholic hepatitis or its progression to cirrhosis. Teratogenic effects can be devastating and are caused by the direct action of ethanol, which inhibits embryonic cellular proliferation early in gestation. This often results in a condition known as fetal alcohol syndrome, which is characterized by craniofacial abnormalities, CNS dysfunction, and both prenatal and postnatal growth retardation in the infant. Pregnant women need to be strongly advised not to consume alcohol during pregnancy, and appropriate treatment and counseling need to be arranged for pregnant women addicted to alcohol or any other drug of abuse.
Interactions
Alcohol can intensify the sedative effects of any medications that work in the CNS (e.g., sedative-hypnotics, benzodiazepines, antidepressants, antipsychotics, opioids). It can interact with the antibiotic metronidazole, causing a disulfiram reaction. Alcohol can also cause severe hepatotoxicity when taken with acetaminophen. Acute ingestion of alcohol can increase the bioavailability of the blood thinner warfarin, which increases the chances of bleeding. Chronic ingestion can cause warfarin to be less effective, leading to increased risks of clots.
Management of Withdrawal, Toxicity, and Overdose
Box 17-6 lists the common signs and symptoms of ethanol withdrawal. Signs and symptoms may vary depending on the individual’s usage pattern, the preferred type of ethanol, and the presence of comorbidities. Treatment of ethanol toxicity is supportive and strives to stabilize the patient and maintain the airway. Ethanol withdrawal can be life threatening.
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